PB0096 - Sera from donors of COVID-19 convalescent plasma do not induce procoagulant phenotype in platelets

Sunday, July 10, 2022

6:30 PM – 7:30 PM

Location: Exhibition

Presentation Format: In-Person

Presenting Author(s)

Günalp Uzun, MD

Physician
Center for Clinical Transfusion Medicine, University Hospital of Tübingen
Tübingen, Baden-Wurttemberg, Germany

Co-Author(s)

Anurag Singh, PhD

Institute for Clinical and Experimental Transfusion Medicine, University Hospital of Tuebingen, Tuebingen, Germany
WA

Wissam Abou-Khalel

Technical Assistant
Institute for Clinical and Experimental Tranfusion Medicine
Tuebingen, Baden-Wurttemberg, Germany
LP

Lisann Pelzl

Post Doc
Institute for Clinical and Experimental Transfusion Medicine, Medical Faculty of Tuebingen, University Hospital of Tuebingen, Tuebingen, Germany
Tuebingen, Baden-Wurttemberg, Germany
KW

Karoline Weich

TA
Institute for clinical and experimental transfusion medicine Tübingen
Tuebingen, Baden-Wurttemberg, Germany
SN

Stefanie Nowak-Harnau

Physician
Center for Clinical Transfusion Medicine
Tübingen, Baden-Wurttemberg, Germany
Karina Althaus, MD

Physician, Director of Platelet Immunology Lab.
Center for Clinical Transfusion Medicine, University Hospital of Tübingen
Tübingen, Baden-Wurttemberg, Germany
PB

Peter Bugert

Professor
Institute of Transfusion Medicine and Immunology, German Red Cross Blood Service Baden-Württemberg – Hessen
Mannheim, Baden-Wurttemberg, Germany
HK

Harald Klüter

Professor
Institute of Transfusion Medicine and Immunology, German Red Cross Blood Service Baden-Württemberg – Hessen
Mannheim, Baden-Wurttemberg, Germany
Tamam Bakchoul, MD

Medical Director
Center for Clinical Transfusion Medicine, University Hospital of Tübingen
Tübingen, Baden-Wurttemberg, Germany

Background: COVID-19 convalescent plasma (CCP) has been suggested to be beneficial to prevent disease progression in COVID-19. However, concerns have been expressed whether plasma components in CCP can shift the already imbalanced coagulation system to a more hypercoagulable state.

Aims: To investigate the effect of CCP on platelet phenotype and activation.

Methods: We investigated platelets from CCP donors who had a history of mild COVID-19 infection. Donors who did not have COVID-19 were used as controls (non-CCP donors). We analyzed phosphatidylserine (PS) externalization, CD62p expression, and GPVI shedding in healthy platelets after incubation with sera from CCP and non-CCP donors using flow cytometry. The study protocol was approved by the ethics committee of the University Hospital of Tübingen.

Results: Forty-seven CCP donors [22 Male, 25 Female; and mean age (±SD) 41.4±13.7 years] with a history of mild COVID-19 infection were included. Median duration after acute COVID-19 infection was 97 days (range, 34-401). Compared to sera from non-CCP donors, sera from CCP donors did not induce higher PS externalization (Fold increase [FI] of PS positive platelets: 1.16% ± 0.66 vs. 1.51% ± 0.74, respectively, p=0.11) or increased the rate of CD62p/PS double positive procoagulant phenotype (FI in CD62p/PS positive platelets: 1.86 ± 0.87 vs. 1.37 ± 0.63, respectively, p=0.10) in platelets from healthy persons. Of note, CD62p expression in healthy platelets after incubation with sera from CCP plasma donors was significantly lower compared to sera from non-CCP donors (FI in CD62p: 2.09 ± 1.36 vs. 1.16 ± 0.45, p< 0.01). Sera-mediated GPVI shedding was similar between non-CCP and CCP donors (1.07 ± 0.16 vs. 1.27 ± 0.91, p=0.52).

Conclusion(s): Our findings support data from clinical studies, which indicate that transfusion of CCP to treat or prevent severe COVID-19 is not associated with increased risk of exacerbation of the coagulopathy in COVID-19.